Tuberculosis is probably as old as mankind. It's continued presence midst us is a sorry tale of missed opportunities and mismanagement by the medical profession.
Pulmonary tuberculosis accounts for eighty five percent of tubercular lesions. One third of the world population of six billion people is infected with Mycobacterium tuberculosis. Only a fraction of them manifest the disease - eight million new cases with three million deaths a year (WHO 1996). It is a national shame that thirty percent of patients of tuberculosis of the world live in India (Pathania et al 1977).
It is estimated that there are two million cases of tuberculosis, In India 85 percent of them with pulmonary tuberculosis and 15 percent extra pulmonary lesions of which 1 to 3 percent are bone and joint lesions. Open, cavitary pulmonary tuberculosis causes the spread of the lesion in the household and the community. Unless these patients are identified and treated effectively, tuberculosis including bone and joint tuberculosis cannot be eradicated.
Bone and Joint tuberculosis results from haematogenous spread from a pulmonary or other visceral or lymph node focus. Great majority of these lesions are healed by nature with one or two foci manifesting themselves from poor nutritional status or lowering of immune responses of the individual.
Till 18th century, tuberculosis was endemic in the community reaching epidemic proportions as "White Plague" on and off. The Industrial Revolution in Europe resulted in improvement of nutrition, sanitation and housing of the poorer sections of the community. That tuberculosis was a 'social disease' was abundantly proved by decreasing incidence with economic well being of the community long before its aetiology was discovered by Robert Koch (1882) or chemotherapeutic drugs specific for Mycobacterium tuberculosis became available in the forties of 20th century. It continues to be a 'social disease' in the developing countries where three quarters of the population of the World live. In the wake of HIV and AIDS and again populations, there is resurgence of tuberculosis in the developed nations of the world also. Unless the governments of the day decide to give up military wars and utilise the enormous resources saved thereby for war on diseases like tuberculosis, there is no likelihood of eradicating tuberculosis.
Long before the discovery of Mycobacterium tuberculosis by Robert Koch (1882), Hippocrates (460-377 B.C.) had suggested a possible relationship between spinal deformity and pulmonary disease. It has been mentioned by others in hymns of Atharva Veda, Dalechamps (1570), Severinus, Percival Pott (1779), Platner (1744) and Jean Pierre David.
Tubercular lesions at other sites were described as follows: tuberculosis osteomyelitis by Nelatoo (1837); histologic morphology by Rokitansky (1884); tuberculosis nodule in a joint by Koster (1869); and synovial tuberculosis by Volkmann (1879).
The discovery of X-rays by William Roentgen in 1895 has given us an invaluable diagnostic tool.
The diagnosis of spinal tuberculosis is not difficult in countries where the disease is common-back pain is the cardinal complaint. A careful observation at the patient as he walks with stiffness of the back, the 'antics' he adopts to lie or get up from the couch gives away the diagnosis. Tenderness over the spinous process and gibbus if present are additional features. Examination of the abdomen for presence of abscess in iliac fossae and a detailed neurological examination complete the examination of the patients. In a sophisticated set-up, the patient is most often fully dressed and already tucked up nicely beneath a bedsheet before the clinician enters the cubicle. At a higher level of sophistication, the clinician does not even see the patient but only MRI films. The standard and cheaper investigations like radiograph, blood counts and ESR will confirm the clinical diagnosis. The more sophisticated and costlier investigations are rarely indicated. But alas, they are ordered indiscriminately for other reasons especially for the rewards they fetch by way of 'kickbacks'. It is hoped that the medical profession stops encouraging such delinquent medibusinesses before the public and the courts disgrace the profession.
The MRC Trials on spinal tuberculosis and clinical practice over several decades have confirmed that in the regions where tuberculosis is prevalent, a clinical diagnosis supported by radiographs is adequate for starting the treatment. However, in early cases, patients with atypical presentation and for cases not responding to chemotherapy, a biopsy may be required.
The treatment had remained empirical-sunlight, fresh air and good food till the advent of chemotherapy in 1940s. With the advent of chemotherapy specific for M. tuberculosis, the natural history of tuberculosis has changed remarkably. With isolation of Streptomycin (Schatz & Waksmann (1944), preparation of Isonicotinic acid hydrazide (Fox 1951), and Para-amino salicylic acid (Lachmann, 1946), triple drug regimens for 12 to 18 months became the standard triple drug therapy.
Mankind had lost a golden opportunity to eradicate tuberculosis in the forties and fifties of the 20th Century. Careless and haphazard management of too little - - too late and inadequate surveillance have resulted in the emergence of drug resistance strains of M. tuberculosis.
Unlike pulmonary tuberculosis, bone and joint tuberculosis is a paucibacillary lesion. Compared to millions of organisms in a cubic centimeter of lung tissue, 100,000 organism in one milliliter of sputum, there are only a million organisms in the entire lesion of spinal tuberculosis. Therefore, if short-course Chemotherapy including rifampicin is effective for pulmonary tuberculosis, it should be equally or more effective for bone and joint tuberculosis.
Madras Study has shown that ambulatory short-course regimen with rifampicin 10 to 15 mgm per kilogram and isoniacid 5 -7 mgm/kg body weight for nine months had favourable results in 99% of patients at 10 year follow-up.
The seminal contributions of Rajasekaran (1999) have not only thrown light on the natural history of lesion but more importantly have provided guidelines for management. The deformity is "dynamic in continuum" leading to correction or deterioration and needs surveillance till the entire growth potential is completed.
The progression of deformity of the spine in tuberculosis passes though three overlapping phases, active phase, growth phase and late phase. While in the adult, the collapse is proportionate to the extent of destruction and stops with consolidation of the lesion, in the child there is an increased collapse for each vertebral loss and may increase or decrease during the growth phase.
Note:In a 15-year follow-up of 63 children below the age of 15 years at the start of the treatment, type I progression was seen in 39%. Therefore the children with type I progression will require surgical treatment.
The clinical features of localisation of tubercular lesions in the joint are pain, muscle spasm, restriction of movements and deformity.
The natural history of tuberculosis of the hip joint seems to depend on the site of the lesion and the duration of the lesion."In 1960s, the author was struck by the lack of correlation between the radiographs and the functional range of movements in these joints. In fact, some of the ghastlylooking radiographs belonged to patients with good range of movements and vice versa. A painstaking study tracing the pre-and post treatment radiographs, age of the patients, the duration of symptoms and the treatment resulted in a "Clinico - Radiological Classification" of seven predictable types of lesions."
These findings have been corroborated by Hoffmann in Cape Town, South of Africa in two historically separated series patients from 1958 on 1978 on triple drug therapy with immobilisation and a second series from 1979 to 1990 with rifampicin ,isoniazide and pyrazinamide either immobilised or mobilised actively or in CPM machines. They concluded that the radiological appearances at presentation was predictable of outcome and that a narrowed joint space was the most reliable sign of poor prognosis, that immobilisation or mobilisation or CPM did not influence the outcome, and that new drugs regimens allowed for shorter treatment but did not appear to influence the outcome (Campbell and Hoffmann 1995).
The lesion is seen in adolescents or in young women soon after childbirth. Antalgic gait is consistently seen which disappears with chemotherapy. Often times the radiographic changes may simulate sacroiliitis of rheumatoid disease but the unilateral involvement and response to treatment will confirm the tuberculosis nature of the lesion. Therefore, the suspicion index must be high for detection and effective treatment of these patients.
Tuberculosis of bones of hand and feet is seen occasionally. While pyogenic organisms especially staphylococcus are mostly responsible for osteomyelitis of long bones, few lesions may be tubercular in nature. Martini et al (1986) have emphasised the importance of biopsies of cases not responding to antibiotics administered based on the culture and sensitivity reports. Tuli has observed tuberculosis infection in 12 patients who had bio-implants or after compound fractures. He has also described immunomodulation techniques for tuberculosis.
Bone and Joint Tuberculosis continues to be prevalent in our country. The diagnosis is not difficult with careful clinical examination and simple and cheap investigations including radiographs. The short-term regimen with rifampicin and isonicotinic acid hydrazide for nine months seems to give good results. The addition of a third drug, ethambutol or pyrazinamide for the first two or three months may prove beneficial. A second opinion from a medical colleague would be rewarding in refractory or resistant lesions. Unnecessary costly investigations are rarely indicated. All efforts should be made to resist temptations by the medibusiness.